Swine with von Willebrand's disease are resistant to development of spontaneous and diet-induced aortic atherosclerosis. The nature of this resistance is unknown. A modern hypothesis suggests that atherosclerosis results from platelet adherence at sites of intimal injury and subsequent release of a platelet derived growth factor for smooth muscle cells. A possible explanation for resistance to atherosclerosis in bleeder pigs, therefore, would be that platelets in these pigs fail to adhere properly at sites of vessel wall injury and do not release the mitogenic factor. The fact that the bleeder pigs are not completely protected from the disease and that there seems to be relatively more atherosclerosis in bleeder pigs in the Chapel Hill colony than in those in the Mayo Clinic colony raises the possibility that factors other than or in addition to the absence of the von Willebrand factor may be involved in the resistance to atherosclerosis enjoyed by these bleeder pigs. To clarfiy this issue, we propose to perform experiments designed to quantify the rate and characteristics of platelet adherence to injured vascular wall and the associated smooth muscle mitogenic activity in bleeder as compared with normal swine. We will examine labelled platelet adherence, ultrastructure, and 3H-thymidine-DNA indices in coronary arteries at various times after balloon injury.